JOY ANNE S. RADAZA.

BSN 2 BARNARD

The Renin-Angiotensin System and Blood Pressure Control

The renin-angiotensin system or RAS regulates blood pressure and fluid
balance in the body. When blood volume or sodium levels in the body are low,
or blood potassium is high, cells in the kidney release the enzyme, renin.
Renin converts angiotensinogen, which is produced in the liver, to the
hormone angiotensin I. An enzyme known as ACE or angiotensin-converting
enzyme found in the lungs metabolizes angiotensin I into angiotensin II.
Angiotensin II causes blood vessels to constrict and blood pressure to
increase. Angiotensin II stimulates the release of the hormone aldosterone in
the adrenal glands, which causes the renal tubules to retain sodium and
water and excrete potassium. Together, angiotensin II and aldosterone work
to raise blood volume, blood pressure and sodium levels in the blood to
restore the balance of sodium, potassium, and fluids. If the
renin-angiotensin system becomes overactive, consistently high blood
pressure results.

Angiotensin II exerts a vasoconstrictive effect on both afferent and efferent arterioles,

but because the efferent arteriole has a smaller basal diameter, the increase in efferent
resistance exceeds the increase in afferent resistance. Afferent vasoconstriction is
further minimized by angiotensin II–mediated release of vasodilatory prostaglandins
and nitric oxide. In addition, angiotensin II can constrict the glomerular mesangium,
thereby reducing the surface area available for filtration.
The net effect of angiotensin II on filtration invokes the opposing factors of reduced
renal blood flow and mesangial surface area (causing a decrease in filtration) and the
increase in glomerular capillary pressure (which tends to increase filtration). The end
result depends on the clinical setting in which it occurs